scholarly journals Thioredoxin Reductase in Human Hepatoma Cells Is Transcriptionally Regulated by Sulforaphane and Other Electrophiles via an Antioxidant Response Element

2003 ◽  
Vol 133 (9) ◽  
pp. 2721-2727 ◽  
Author(s):  
Korry J. Hintze ◽  
Karl A. Wald ◽  
Huawei Zeng ◽  
Elizabeth H. Jeffery ◽  
John W. Finley
Keyword(s):  
Thioredoxin Reductase ◽  
Antioxidant Response ◽  
Hepatoma Cells ◽  
Antioxidant Response Element ◽  
Human Hepatoma ◽  
Human Hepatoma Cells ◽  
Response Element

NF-AB, a liver-specific and cytokine-inducible nuclear factor that interacts with the interleukin-1 response element of the rat alpha 1-acid glycoprotein gene

1991 ◽  
Vol 11 (6) ◽  
pp. 3001-3008
Author(s):  
K A Won ◽  
H Baumann
Keyword(s):  
Dna Sequence ◽  
Phorbol Ester ◽  
Interleukin 1 ◽  
Hepatoma Cells ◽  
Binding Activity ◽  
Nuclear Factor ◽  
Human Hepatoma ◽  
Human Hepatoma Cells ◽  
Response Element ◽  
Acid Glycoprotein

The 142-bp cytokine response element of the rat alpha 1-acid glycoprotein (AGP) gene is a complex of several additively contributing regulatory sequences. By using deletions and point mutations, a minimal interleukin-1 (IL-1) response element was localized to the region from positions 1 to 36 within the 5'-most AB fragment of the cytokine response element. Two distinct sequence motifs were contained within this element, both of which were required to achieve full IL-1 response in rat and human hepatoma cells. This element showed a minor response to phorbol ester treatment only in human hepatoma cells. Southwestern (DNA-protein) blot analysis of nuclear proteins of rat liver and hepatoma cells revealed the presence of a heat-labile nuclear factor (NF-AB). NF-AB migrated as a basic protein with an apparent molecular mass of 37 kDa and bound specifically to the DNA sequence at positions 10 to 37 of the AB fragment. The NF-AB binding activity was detected neither in the cytoplasmic fraction of rat hepatoma cells nor in nuclear extracts from control or acute-phase rat kidney. The binding activity of NF-AB correlated with the transcriptional activity of the endogenous AGP gene in rat liver and hepatoma cells. Nuclear extract from human HepG2 cells showed a similar binding activity with an apparent molecular mass of 34.5 kDa. The human NF-AB binding activity was detectable only after 13 h of cytokine treatment and was not induced by phorbol ester. Tissue distribution, DNA sequence binding specificity, and kinetics of cytokine induction of NF-AB do not coincide with the characteristics of any other described factors that have been associated with cytokine regulation. Therefore, NF-AB is considered a new candidate involved in IL-1 regulation of the rat AGP gene.

scholarly journals NF-AB, a liver-specific and cytokine-inducible nuclear factor that interacts with the interleukin-1 response element of the rat alpha 1-acid glycoprotein gene.

1991 ◽  
Vol 11 (6) ◽  
pp. 3001-3008 ◽  
Author(s):  
K A Won ◽  
H Baumann
Keyword(s):  
Dna Sequence ◽  
Phorbol Ester ◽  
Interleukin 1 ◽  
Hepatoma Cells ◽  
Binding Activity ◽  
Nuclear Factor ◽  
Human Hepatoma ◽  
Human Hepatoma Cells ◽  
Response Element ◽  
Acid Glycoprotein

The 142-bp cytokine response element of the rat alpha 1-acid glycoprotein (AGP) gene is a complex of several additively contributing regulatory sequences. By using deletions and point mutations, a minimal interleukin-1 (IL-1) response element was localized to the region from positions 1 to 36 within the 5'-most AB fragment of the cytokine response element. Two distinct sequence motifs were contained within this element, both of which were required to achieve full IL-1 response in rat and human hepatoma cells. This element showed a minor response to phorbol ester treatment only in human hepatoma cells. Southwestern (DNA-protein) blot analysis of nuclear proteins of rat liver and hepatoma cells revealed the presence of a heat-labile nuclear factor (NF-AB). NF-AB migrated as a basic protein with an apparent molecular mass of 37 kDa and bound specifically to the DNA sequence at positions 10 to 37 of the AB fragment. The NF-AB binding activity was detected neither in the cytoplasmic fraction of rat hepatoma cells nor in nuclear extracts from control or acute-phase rat kidney. The binding activity of NF-AB correlated with the transcriptional activity of the endogenous AGP gene in rat liver and hepatoma cells. Nuclear extract from human HepG2 cells showed a similar binding activity with an apparent molecular mass of 34.5 kDa. The human NF-AB binding activity was detectable only after 13 h of cytokine treatment and was not induced by phorbol ester. Tissue distribution, DNA sequence binding specificity, and kinetics of cytokine induction of NF-AB do not coincide with the characteristics of any other described factors that have been associated with cytokine regulation. Therefore, NF-AB is considered a new candidate involved in IL-1 regulation of the rat AGP gene.

The KLF6 Super Enhancer Modulates Cell Proliferation via MiR-1301 in Human Hepatoma Cells

MicroRNA ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 64-69 ◽  
Author(s):  
KumChol Ri ◽  
Chol Kim ◽  
CholJin Pak ◽  
PhyongChol Ri ◽  
HyonChol Om
Keyword(s):  
Cell Proliferation ◽  
Cellular Proliferation ◽  
Hepatoma Cells ◽  
Regulation Mechanism ◽  
Dependent Manner ◽  
Human Hepatoma ◽  
Human Hepatoma Cells ◽  
Over Expression ◽  
Super Enhancer ◽  
Engineering Changes

Background: Recent studies have attempted to elucidate the function of super enhancers by means of microRNAs. Although the functional outcomes of miR-1301 have become clearer, the pathways that regulate the expressions of miR-1301 remain unclear. Objective: The objective of this paper was to consider the pathway regulating expression of miR- 1301 and miR-1301 signaling pathways with the inhibition of cell proliferation. Methods: In this study, we prepared the cell clones that the KLF6 super enhancer was deleted by means of the CRISPR/Cas9 system-mediated genetic engineering. Changes in miR-1301 expression after the deletion of the KLF6 super enhancer were evaluated by RT-PCR analysis, and the signal pathway of miR-1301 with inhibition of the cell proliferation was examined using RNA interference technology. Results: The results showed that miR-1301 expression was significantly increased after the deletion of the KLF6 super enhancer. Over-expression of miR-1301 induced by deletion of the KLF6 super enhancer also regulated the expression of p21 and p53 in human hepatoma cells. functional modeling of findings using siRNA specific to miR-1301 showed that expression level changes had direct biological effects on cellular proliferation in Human hepatoma cells. Furthermore, cellular proliferation assay was shown to be directly associated with miR-1301 levels. Conclusion: As a result, it was demonstrated that the over-expression of miR-1301 induced by the disruption of the KLF6 super enhancer leads to a significant inhibition of proliferation in HepG2 cells. Moreover, it was demonstrated that the KLF6 super enhancer regulates the cell-proliferative effects which are mediated, at least in part, by the induction of p21and p53 in a p53-dependent manner. Our results provide the functional significance of miR-1301 in understanding the transcriptional regulation mechanism of the KLF6 super enhancer.

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